scholarly journals Intectin, a Novel Small Intestine-specific Glycosylphosphatidylinositol-anchored Protein, Accelerates Apoptosis of Intestinal Epithelial Cells

2004 ◽  
Vol 279 (41) ◽  
pp. 42867-42874 ◽  
Author(s):  
Hidefumi Kitazawa ◽  
Tamao Nishihara ◽  
Tadahiro Nambu ◽  
Hitoshi Nishizawa ◽  
Masanori Iwaki ◽  
...  
Keyword(s):  
Small Intestine ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial

Effect of leptin on intestinal apolipoprotein AIV in response to lipid feeding

2001 ◽  
Vol 281 (3) ◽  
pp. R753-R759 ◽  
Author(s):  
Takashi Doi ◽  
Min Liu ◽  
Randy J. Seeley ◽  
Stephen C. Woods ◽  
Patrick Tso
Keyword(s):  
Small Intestine ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Regional Distribution ◽  
Intestinal Epithelial ◽  
Lipid Infusion ◽  
Intraduodenal Infusion ◽  
Crypt Cells

We determined apolipoprotein AIV (apo AIV) content in intestinal epithelial cells using immunohistochemistry when leptin was administered intravenously. Most of the apo AIV immunoreactivity in the untreated intestine was located in the villous cells as opposed to the crypt cells. Regional distribution of apo AIV immunostaining revealed low apo AIV content in the duodenum and high content in the jejunum that gradually decreases caudally toward the ileum. Intraduodenal infusion of lipid (4 h) significantly increased apo AIV immunoreactivity in the jejunum and ileum. Simultaneous intravenous leptin infusion plus duodenal lipid infusion markedly suppressed apo AIV immunoreactivity. Duodenal lipid infusion increased plasma apo AIV significantly (measured by ELISA), whereas simultaneous leptin infusion attenuated the increase. These findings suggest that leptin may regulate circulating apo AIV by suppressing apo AIV synthesis in the small intestine.

scholarly journals Role of Intestinal Epithelial Cells in Immune Effects Mediated by Gram-Positive Probiotic Bacteria: Involvement of Toll-Like Receptors

2005 ◽  
Vol 12 (9) ◽  
pp. 1075-1084 ◽  
Author(s):  
Gabriel Vinderola ◽  
Chantal Matar ◽  
Gabriela Perdigon
Keyword(s):  
Small Intestine ◽  
B Cells ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Primary Cultures ◽  
Clonal Expansion ◽  
Probiotic Bacteria ◽  
Intestinal Epithelial ◽  
Toll Like Receptors

ABSTRACT The mechanisms by which probiotic bacteria exert their effects on the immune system are not completely understood, but the epithelium may be a crucial player in the orchestration of the effects induced. In a previous work, we observed that some orally administered strains of lactic acid bacteria (LAB) increased the number of immunoglobulin A (IgA)-producing cells in the small intestine without a concomitant increase in the CD4+ T-cell population, indicating that some LAB strains induce clonal expansion only of B cells triggered to produce IgA. The present work aimed to study the cytokines induced by the interaction of probiotic LAB with murine intestinal epithelial cells (IEC) in healthy animals. We focused our investigation mainly on the secretion of interleukin 6 (IL-6) necessary for the clonal expansion of B cells previously observed with probiotic bacteria. The role of Toll-like receptors (TLRs) in such interaction was also addressed. The cytokines released by primary cultures of IEC in animals fed with Lactobacillus casei CRL 431 or Lactobacillus helveticus R389 were determined. Cytokines were also determined in the supernatants of primary cultures of IEC of unfed animals challenged with different concentrations of viable or nonviable lactobacilli and Escherichia coli, previously blocked or not with anti-TLR2 and anti-TLR4. We concluded that the small intestine is the place where a major distinction would occur between probiotic LAB and pathogens. This distinction comprises the type of cytokines released and the magnitude of the response, cutting across the line that separates IL-6 necessary for B-cell differentiation, which was the case with probiotic lactobacilli, from inflammatory levels of IL-6 for pathogens.

Suppressor of cytokine signaling-2 limits intestinal growth and enterotrophic actions of IGF-I in vivo

2006 ◽  
Vol 291 (3) ◽  
pp. G472-G481 ◽  
Author(s):  
Carmen Z. Michaylira ◽  
James G. Simmons ◽  
Nicole M. Ramocki ◽  
Brooks P. Scull ◽  
Kirk K. McNaughton ◽  
...  
Keyword(s):  
Small Intestine ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Ex Vivo ◽  
Cytokine Signaling ◽  
Intestinal Epithelial ◽  
Growth Responses ◽  
Intestinal Growth ◽  
Igf I

Suppressors of cytokine signaling (SOCS) typically limit cytokine receptor signaling via the JAK-STAT pathway. Considerable evidence demonstrates that SOCS2 limits growth hormone (GH) action on body and organ growth. Biochemical evidence that SOCS2 binds to the IGF-I receptor (IGF-IR) supports the novel possibility that SOCS2 limits IGF-I action. The current study tested the hypothesis that SOCS2 normally limits basal or IGF-I-induced intestinal growth and limits IGF-IR signaling in intestinal epithelial cells. Intestinal growth was assessed in mice homozygous for SOCS2 gene deletion (SOCS2 null) and wild-type (WT) littermates at different ages and in response to infused IGF-I or vehicle or EGF and vehicle. The effects of SOCS2 on IGF-IR signaling were examined in ex vivo cultures of SOCS2 null and WT intestine and Caco-2 cells. Compared with WT, SOCS2 null mice showed significantly enhanced small intestine and colon growth, mucosal mass, and crypt cell proliferation and decreases in radiation-induced crypt apoptosis in jejunum. SOCS2 null mice showed significantly greater growth responses to IGF-I in small intestine and colon. IGF-I-stimulated activation of IGF-IR and downstream signaling intermediates were enhanced in the intestine of SOCS2 null mice and were decreased by SOCS2 overexpression in Caco-2 cells. SOCS2 bound directly to the endogenous IGF-IR in Caco-2 cells. The intestine of SOCS2 null mice also showed enhanced growth responses to infused EGF. We conclude that SOCS2 normally limits basal and IGF-I- and EGF-induced intestinal growth in vivo and has novel inhibitory effects on the IGF-IR tyrosine kinase pathway in intestinal epithelial cells.

scholarly journals Immunocytochemical localization of ornithine transcarbamylase in rat intestinal mucosa. Light and electron microscopic study.

1988 ◽  
Vol 36 (1) ◽  
pp. 29-35 ◽  
Author(s):  
Y Hamano ◽  
H Kodama ◽  
M Yanagisawa ◽  
Y Haraguchi ◽  
M Mori ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Small Intestine ◽  
Epithelial Cells ◽  
Light Microscopy ◽  
Intestinal Mucosa ◽  
Intestinal Epithelial Cells ◽  
Protein A ◽  
Intestinal Epithelial ◽  
Electron Microscopic ◽  
Small Intestinal

We investigated light and electron microscopic localization of ornithine transcarbamylase (OTC) in rat intestinal mucosa. In the immunoblotting assay of OTC-related protein, a single protein band with a molecular weight of about 36,500 is observed in extracts of liver and small intestinal mucosa but is not observed in those of stomach and large intestine. For light microscopy, tissue slices of the digestive system were embedded in Epon and stained by using anti-bovine OTC rabbit IgG and the immunoenzyme technique. For electron microscopy, slices of these and the liver tissues were embedded in Lowicryl K4M and stained by the protein A-gold technique. By light microscopy, the absorptive epithelial cells of duodenum, jejunum, and ileum stained positively for OTC, but stomach, large intestine, rectum, and propria mucosa of small intestine were not stained. Electron microscopy showed that gold particles representing the antigenic sites for OTC were confined to the mitochondrial matrix of hepatocytes and small intestinal epithelial cells. However, the enzyme was detected in mitochondria of neither liver endothelial cells, submucosal cells of small intestine, nor large intestinal epithelial cells. Labeling density of mitochondria in the absorptive epithelial cells of duodenum, jejunum, and ileum was about half of that in liver cells.

Functional involvement of RFVT3/SLC52A3 in intestinal riboflavin absorption

2014 ◽  
Vol 306 (2) ◽  
pp. G102-G110 ◽  
Author(s):  
Hiroki Yoshimatsu ◽  
Atsushi Yonezawa ◽  
Yoshiaki Yao ◽  
Kumiko Sugano ◽  
Shunsaku Nakagawa ◽  
...  
Keyword(s):  
Methylene Blue ◽  
Small Intestine ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Biological Membrane ◽  
Transport Systems ◽  
Intestinal Epithelial ◽  
T84 Cells ◽  
Functional Involvement ◽  
Apical Membranes

Riboflavin, also known as vitamin B2, is transported across the biological membrane into various organs by transport systems. Riboflavin transporter RFVT3 is expressed in the small intestine and has been suggested to localize in the apical membranes of the intestinal epithelial cells. In this study, we investigated the functional involvement of RFVT3 in riboflavin absorption using intestinal epithelial T84 cells and mouse small intestine. T84 cells expressed RFVT3 and conserved unidirectional riboflavin transport corresponding to intestinal absorption. Apical [3H]riboflavin uptake was pH-dependent in T84 cells. This uptake was not affected by Na+ depletion at apical pH 6.0, although it was significantly decreased at apical pH 7.4. The [3H]riboflavin uptake from the apical side of T84 cells was prominently inhibited by the RFVT3 selective inhibitor methylene blue and significantly decreased by transfection of RFVT3-small-interfering RNA. In the gastrointestinal tract, RFVT3 was expressed in the jejunum and ileum. Mouse jejunal and ileal permeabilities of [3H]riboflavin were measured by the in situ closed-loop method and were significantly reduced by methylene blue. These results strongly suggest that RFVT3 would functionally be involved in riboflavin absorption in the apical membranes of intestinal epithelial cells.

scholarly journals Small intestine barrier function failure induces systemic inflammation in monosodium glutamate-induced chronically obese mice

2019 ◽  
Vol 44 (6) ◽  
pp. 587-594 ◽  
Author(s):  
Kazuhiko Nakadate ◽  
Tomoya Hirakawa ◽  
Sawako Tanaka-Nakadate
Keyword(s):  
Small Intestine ◽  
Epithelial Cells ◽  
Systemic Inflammation ◽  
Intestinal Epithelial Cells ◽  
Monosodium Glutamate ◽  
Intestinal Epithelial ◽  
Obese Mice ◽  
Gastrointestinal Barrier ◽  
Small Intestinal ◽  
Functional Deterioration

Chronic obesity has increased worldwide, in conjunction with type 2 diabetes. Chronic obesity causes systemic inflammation that may result in functional deterioration of the gastrointestinal barrier. However, gastrointestinal conditions associated with chronic obesity have not been comprehensively investigated. The purpose of this study was to evaluate morphological changes in small intestine barrier structures during chronic obesity. A mouse model of chronic obesity induced by monosodium glutamate treatment was established. At postnatal week 15, pathological changes including in small intestinal epithelial cells were analyzed in chronically obese mice compared with controls. Numerous gaps were identified between small intestinal epithelial cells in chronically obese mice, and levels of both desmosomal and tight junction proteins were significantly lower in their small intestinal epithelial cells. Moreover, in chronically obese mice, a significant increase in the number of intestinal inflammatory cells, particularly macrophages, was observed; in addition, blood samples from the mouse model show an increase in markers of inflammation, tumor necrosis factor-alpha and interleukin-1-beta. These findings suggest that functional deterioration of adhesion structures between small intestinal epithelial cells causes gastrointestinal barrier function failure, leading to a rise in intestinal permeability to blood vessels and consequent systemic inflammation, characterized by macrophage infiltration.

ISOLATION OF THE EPITHELIAL CELLS OF THE RAT SMALL INTESTINE

1966 ◽  
Vol 44 (6) ◽  
pp. 687-693 ◽  
Author(s):  
A. D. Perris
Keyword(s):  
Small Intestine ◽  
Epithelial Cells ◽  
Linear Relationship ◽  
Incubation Medium ◽  
Intestinal Epithelial Cells ◽  
Cellular Level ◽  
New Method ◽  
Intestinal Epithelial ◽  
Rat Small Intestine ◽  
Intestinal Function

A new method for the preparation of isolated intestinal epithelial cells from the rat is described. Suspensions of these cells respire actively, taking up oxygen in a linear relationship with time for about 40 minutes. When actively transported sugars are present in the incubation medium, the cells utilize more oxygen. It is suggested that such preparations may be useful in the study of intestinal function at the cellular level.

scholarly journals 62 Evaluating detoxification efficacy of deoxynivalenol by encapsulated sodium metabisulfite (SMBS) using an in vitro intestinal epithelial cell IPEC-J2 model

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 38-39
Author(s):  
Peng Lu ◽  
Changning Yu ◽  
Shangxi Liu ◽  
Joshua Gong ◽  
Song Liu ◽  
...  
Keyword(s):  
Small Intestine ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial Cells ◽  
In Vitro Release ◽  
Simulated Gastric Fluid ◽  
Sodium Metabisulfite ◽  
Intestinal Epithelial

Abstract Deoxynivalenol (DON) contamination occurs on feed ingredients and causes a reduction in growth performance, damage to the intestinal epithelial cells, and increased susceptibility to enteric pathogen challenge. Sodium metabisulfite (SMBS) has been successfully used to destroy DON in processed grains or feeds. However, SMBS degrades quickly under aqueous acid conditions, such as pig stomachs, and when SMBS is added to diet, little will remain intact in the small intestine where an optimal pH environment exists for detoxification by SMBS. Thus, this study was to encapsulate SMBS into microparticles to deliver intact SMBS to the small intestine and evaluate its efficacy of DON detoxification in the simulated intestine fluid (SIF) using an in vitro intestinal epithelial cell (IPEC-J2) model. The results showed that around 40% of the SMBS loading capacity was achieved in the microparticles. In vitro release studies showed that 1.61% of encapsulated SMBS was released in the simulated gastric fluid (SGF), and the majority of encapsulated SMBS (75.52%) was progressively released in the SIF within 6 h at 37 °C. In vitro cell experiments showed that DON treated with the SIF containing 0.5% SMBS for 2 h completely attenuated the DON-induced cytotoxicity. When DON was treated with the SGF containing 0.5% encapsulated SMBS for 2 h and then the mixture was mixed with the SIF (1:1) and incubated for 2 h, it also completely attenuated the DON-induced cytotoxicity. Moreover, DON treated with the simulated fluid containing 0.5% encapsulated SMBS completely attenuated the gene expression inflammatory cytokines upregulated by DON and restored trans-epithelial electrical resistance (TEER) and tight junction and cytoskeleton. In summary, the encapsulation of SMBS was stable in SGF and allowed a progressive release of SMBS in the SIF. Moreover, the released SMBS in the SIF effectively attenuated the adverse effects induced by DON in the intestinal epithelial cells.

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